Abstract
In pancreatic acinar cells, agonists evoke intracellular Ca(2+) transients which are initiated in the apical region of these polarized cells. There are contradictory experimental data concerning Ca(2+) release from ryanodine receptors (RyRs) in the apical region. In the present study, we have used low doses of ryanodine to open RyRs leading to the release of Ca(2+) from intracellular stores. Ryanodine causes Ca(2+) release that is initiated in the apical region of the cell but is dependent upon functional inositol 1,4,5-trisphosphate receptors (IP(3)Rs). These results suggests that co-ordinated release from co-localized RyRs and IP(3)Rs underlies the increased sensitivity of the apical region to initiation of intracellular Ca(2+) transients.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Caffeine / pharmacology
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Calcium / metabolism*
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Calcium Channels / drug effects
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Calcium Channels / metabolism
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Cells, Cultured
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Dose-Response Relationship, Drug
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Inositol 1,4,5-Trisphosphate Receptors
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Mice
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Pancreas / cytology
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Pancreas / drug effects
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Pancreas / metabolism*
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Receptors, Cytoplasmic and Nuclear / drug effects
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Receptors, Cytoplasmic and Nuclear / metabolism
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Ryanodine / pharmacology*
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Ryanodine Receptor Calcium Release Channel / drug effects
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Ryanodine Receptor Calcium Release Channel / metabolism
Substances
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Calcium Channels
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Inositol 1,4,5-Trisphosphate Receptors
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Receptors, Cytoplasmic and Nuclear
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Ryanodine Receptor Calcium Release Channel
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Ryanodine
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Caffeine
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Calcium